Recent study results on the association between maternal exposure to ambient air pollution with preterm birth have been inconsistent. The sensitive window of exposure and influence level of air pollutants varied greatly. We aimed to explore the association between maternal exposure to ambient air pollutants and the risk of preterm birth, and to estimate the sensitive exposure time window. A total of 572,116 mother–newborn pairs, daily concentrations of air pollutants from nearest monitoring stations were used to estimate exposures for each participant during 2015–2020 in Chongqing, China. We applied a generalized additive model and estimated RRs and 95% CIs for preterm birth in each trimester and the entire pregnancy period. In the single-pollutant model, we observed that each 10 μg/m3 increase in PM2.5 had a statistically significant effect on the third trimester and entire pregnancy, with RR = 1.036 (95% CI: 1.021, 1.051) and RR = 1.101 (95% CI: 1.075, 1.128), respectively. Similarly, for each 10 μg/m3 increase in PM10, there were 2.7% (RR = 1.027, 95% CI: 1.016, 1.038) increase for PTB on the third trimester, and 3.8% (RR = 1.038, 95% CI: 1.020, 1.057) increase during the whole pregnancy. We found that for each 10 mg/m3 CO increases, the relative risk of PTB increased on the first trimester (RR = 1.081, 95% CI: 1.007, 1.162), second trimester (RR = 1.116, 95% CI: 1.035, 1.204), third trimester (RR = 1.167, 95% CI: 1.090, 1.250) and whole pregnancy (RR = 1.098, 95% CI: 1.011, 1.192). No statistically significant RR was found for SO2 and NO2 on each trimester of pregnancy. Our study indicates that maternal exposure to high levels of PM2.5 and PM10 during pregnancy may increase the risk for preterm birth, especially for women at the late stage of pregnancy. Statistically increased risks of preterm birth were associated with CO exposure during each trimester and entire pregnancy. Reducing exposure to ambient air pollutants for pregnant women is clearly necessary to improve the health of infants.

Introduction Recent studies demonstrated that living in areas with high ambient air pollution may have adverse effects on pregnancy outcomes, but few studies have investigated its association with spontaneous abortion. Further investigation is needed to explore the acute effect and lag effect of air pollutants exposure on spontaneous abortion. Objective To investigate the acute effect and lag effect between exposure to ambient air pollutants and spontaneous abortion. Methods Research data of spontaneous abortion were collected from the Chongqing Health Center for Women and Children (CQHCWC) in China. The daily ambient air pollution exposure measurements were estimated for each woman using inverse distance weighting from monitoring stations. A time-stratified, case-crossover design combined with distributed lag linear models was applied to assess the associations between spontaneous pregnancy loss and exposure to each of the air pollutants over lags 0–7 days, adjusted for temperature and relative humidity. Results A total of 1399 women who experienced spontaneous pregnancy loss events from November 1, 2016, to September 30, 2019, were selected for this study. Maternal exposure to particulate matter 2.5 (PM2.5), particle matter 10 (PM10) nitrogen dioxide (NO2), and sulfur dioxide (SO2) exhibited a significant association with spontaneous abortion. For every 20 μg/m3 increase in PM2.5, PM10, NO2, and SO2, the RRs were 1.18 (95% CI: 1.06, 1.34), 1.12 (95% CI, 1.04–1.20), 1.15 (95% CI: 1.02, 1.30), and 1.92 (95% CI: 1.18, 3.11) on lag day 3, lag day 3, lag day 0, and lag day 3, respectively. In two-pollutant model combined with PM2.5 and PM10, a statistically significant increase in spontaneous abortion incidence of 18.0% (RR = 1.18, 95% CI: 1.06, 1.32) was found for a 20 μg/m3 increase in PM2.5 exposure, and 11.2% (RR = 1.11, 95% CI: 1.03, 1.20) for a 20 μg/m3 increase in PM10 exposure on lag day 3, similar to single-pollutant model analysis. Conclusion Maternal exposure to high levels of PM2.5, PM10, NO2, and SO2 during pregnancy may increase the risk of spontaneous abortion for acute effects and lag effects. Further research to explore sensitive exposure time windows is needed.

For patients with platinum-resistant lung adenocarcinoma (LUAD), the exploration of new effective drug candidates is urgently needed. Fibroblast growth factor receptors (FGFRs) have been identified as promising targets for LUAD therapy. The purpose of this study was to determine the exact role of the irreversible FGFR1-4 inhibitor FIIN-2 in LUAD and to clarify its underlying molecular mechanisms. Our results demonstrated that FIIN-2 significantly inhibited the proliferation, colony formation, and migration of A549 and A549/DDP cells but induced the mitochondria-mediated apoptosis of these cells. Meanwhile, FIIN-2 increased the autophagy flux of A549 and A549/DDP cells by inhibiting the mammalian target of rapamycin (mTOR) and further activating the class III PI3K complex pathway. More importantly, in vivo and in vitro experiments showed that autophagy inhibitors could enhance the cytotoxicity of FIIN-2 on A549 and A549/DDP cells, confirming that FIIN-2 induced protective autophagy. These findings indicated that FIIN-2 is a potential drug candidate for LUAD treatment, and its use in combination with autophagy inhibitors might be an efficient treatment strategy, especially for patients with cisplatin resistance.

The objective of this study was to evaluate the risk factors, pathogenic bacteria and drug sensitivity of maternal sepsis, and provide evidence for clinical prevention and treatment. A retrospective investigation of pregnant women with full-term maternal sepsis was performed to analyze the risk factors, pathogenic bacteria, and drug sensitivity of maternal sepsis. Univariate analysis showed that temperature, serum procalcitonin (PCT) and C-reactive protein (CRP) at admission, white blood cell count (WBC), PCT, CRP and neutrophilic granulocyte percentage (N%) during fever, premature rupture of membranes (PROM), antibiotic use within 1 week, mode of production, onset and duration of fever, between groups were statistically significant (P < .05). Logistic regression analysis showed that cesarean section was an independent risk factor for sepsis (OR = 11.839, 95%CI: 3.121–44.906). Apparent increase was found in body temperature (OR = 3.664, 95%CI: 1.722–7.795), duration of fever (OR = 1.953, 95%CI: 1.242–3.071), and PCT (OR = 1.080, 95%CI: 1.002–1.163). Also, increasing neutrophil ratio (OR = 1.180, 95%CI: 1.073–1.297) indicated a high possibility of maternal sepsis. The organism Escherichia coli (E. coli) was the most common pathogenic bacteria in the positive blood culture group (90%), and the sensitivity to carbapenems (meropenem and imipenem/cilastatin) was 100%, that to piperacillin-tazobactam and amoxicillin sulbactam was over 90%, and that to ceftazidime was 95%. Cesarean section was an independent risk factor for maternal sepsis in term pregnant women with positive blood culture. Besides, the E. coli was the most common pathogenic bacteria in the positive blood culture group. Antibiotics should be used in time and reasonably when the temperature was significantly increased with elevated PCT and N% after a cesarean section.

Context Polyphyllin II (PPII) is a steroidal saponin isolated from Rhizoma Paridis . It exhibits significant antitumor activity such as anti-proliferation and pro-apoptosis in lung cancer. Objective To explore whether PPII induce autophagy and the relationship between autophagy and apoptosis in non-small cell lung cancer (NSCLC) cells. Materials and methods The effects of PPII (0, 1, 5, and 10 μM) were elucidated by CCK8 assay, colony formation test, TUNEL staining, MDC method, and mRFP-GFP-LC3 lentivirus transfection in A549 and H1299 cells for 24 h. DMSO-treated cells were selected as control. The protein expression of autophagy (LC3-II, p62), apoptosis (Bcl-2, Bax, caspase-3) and p-mTOR was detected by Western blotting. We explored the relationship between autophagy and apoptosis by autophagy inhibitor CQ (10 μM) and 3-MA (5 mM). Results PPII (0, 1, 5, and 10 μM) inhibited the proliferation and induced apoptosis. The IC 50 values of A549 and H1299 cells were 8.26 ± 0.03 and 2.86 ± 0.83 μM. We found that PPII could induce autophagy. PPII promoted the formation of autophagosome, increased the expression of LC3-II/LC3-I ( p < 0.05), while decreased p62 and p-mTOR ( p < 0.05). Additionally, the co-treatment with autophagy inhibitors promoted the protein expression of c-caspase-3 and rate of Bax/Bcl-2 ( p < 0.05), compared with PPII-only treatment group. Therefore, our results indicated that PPII-induced autophagy may be a mechanism to promote cell survival, although it can also induce apoptosis. Conclusions PPII-induced apoptosis exerts its anticancer activity by inhibiting autophagy, which will hopefully provide a prospective compound for NSCLC treatment.

IntroductionThere have been many researches done on the association between maternal exposure to ambient air pollution and adverse pregnancy outcomes, but few studies related to very low birth weight (VLBW). This study thus explores the association between maternal exposure to ambient air pollutants and the risk of VLBW, and estimates the sensitive exposure time window.MethodsA retrospective cohort study analyzed in Chongqing, China, during 2015–2020. The Generalized Additive Model were applied to estimate exposures for each participant during each trimester and the entire pregnancy period.ResultsFor each 10 μg/m3 increase in PM2.5 during pregnancy, the relative risk of VLBW increased on the first trimester, with RR = 1.100 (95% CI: 1.012, 1.195) in the single-pollutant model. Similarly, for each 10 μg/m3 increase in PM10, there was a 12.9% (RR = 1.129, 95% CI: 1.055, 1.209) increase for VLBW on the first trimester in the single-pollutant model, and an 11.5% (RR = 1.115, 95% CI: 1.024, 1.213) increase in the multi-pollutant model, respectively. The first and second trimester exposures of NO2 were found to have statistically significant RR values for VLBW. The RR values on the first trimester were 1.131 (95% CI: 1.037, 1.233) and 1.112 (95% CI: 1.015, 1.218) in the single-pollutant model and multi-pollutant model, respectively; The RR values on the second trimester were 1.129 (95% CI: 1.027, 1.241) and 1.146 (95% CI: 1.038, 1.265) in the single-pollutant model and multi-pollutant model, respectively. The RR of O3 exposure for VLBW on the entire trimester was 1.076 (95% CI: 1.010–1.146), and on the second trimester was 1.078 (95% CI: 1:016, 1.144) in the single-pollutant model.ConclusionThis study indicates that maternal exposure to high levels of PM2.5, PM10, NO2, and O3 during pregnancy may increase the risk of very low birth weight, especially for exposure on the first and second trimester. Reducing the risk of early maternal exposure to ambient air pollution is thus necessary for pregnant women.

Accumulating evidence suggested that the risk of preterm births (PTBs) following prenatal exposure to air pollution was inconclusive. The aim of this study is to investigate the relationship between air pollution exposure in the days before delivery and PTB and assess the threshold effect of short-term prenatal exposure to air pollution on PTB. This study collected data including meteorological factors, air pollutants, and information in Birth Certificate System from 9 districts during 2015–2020 in Chongqing, China. Generalized additive models (GAMs) with the distributed lag non-linear models were conducted to assess the acute impact of air pollutants on the daily counts of PTB, after controlling for potential confounding factors. We observed that PM2.5 was related to increased occurrence of PTB on lag 0–3 and lag 10–21 days, with the strongest on the first day (RR = 1.017, 95%CI: 1.000–1.034) and then decreasing. The thresholds of PM2.5 for lag 1–7 and 1–30 days were 100 μg/m3 and 50 μg/m3, respectively. The lag effect of PM10 on PTB was very similar to that of PM2.5. In addition, the lagged and cumulative exposure of SO2 and NO2 was also associated with the increased risk of PTB. The lag relative risk and cumulative relative risk of CO exposure were the strongest, with a maximum RR at lag 0 (RR = 1.044, 95%CI: 1.018, 1.069). Importantly, the exposure–response curve of CO showed that RR increased rapidly when the concentration exceeded 1000 μg/m3. This study indicated significant associations between air pollution and PTB. The relative risk decreases with day lag, while the cumulative effect increases. Thus, pregnant women should understand the risk of air pollution and try to avoid high concentration exposure.

Background: The resistance rate of carbapenem-resistant Enterobacteriaceae (CRE) is increasing yearly but rarely reported in children. Objectives: This retrospective study analyzed the characteristics of isolated CRE strains in pediatric patients, intending to explore reasonable antimicrobial treatment options. Methods: Some CRE isolates were collected from infected pediatric patients in Liaocheng People’s Hospital from January 2014 to December 2019. The strain identification and antimicrobial susceptibility testing were conducted using Vitek mass spectrometry and the Vitek 2 system, respectively. The carbapenemase genotypes of blaKPC, blaIMP, blaVIM, blaNDM-1, and blaOXA-48 were each detected by polymerase chain reaction and sequencing. The molecular homology analysis of strains was conducted via Pulse-field Gel Electrophoresis (PFGE). The clinical data of CRE-infected pediatric patients were collected from the hospital’s medical data information system. Results: Twenty CRE strains were isolated from 1945 infected pediatric patients with Enterobacteriaceae. All CRE strains showed multiple resistance to commonly used antimicrobials. Twelve strains of imipenemase (IMP)-4 and seven strains of IMP-8 carbapenemase were confirmed. Besides, PFGE revealed that two strains of Escherichia coli and three of Klebsiella pneumoniae had indistinguishable patterns. Sixteen patients were cured, including 10 patients using piperacillin/tazobactam. Conclusions: This study found the major sources of resistance were IMP carbapenemases. Piperacillin/tazobactam is potentially effective for the treatment of CRE infection, despite insensitivity in vitro.